Low birth weight in response to salt restriction during pregnancy is not due to alterations in uterine-placental blood flow or the placental and peripheral renin–angiotensin system

• Published in: Physiology & behavior 2008-09, Vol.95 (1), p.145-151
• Main Authors: Leandro, Sandra Márcia, Furukawa, Luzia Naôko Shinohara, Shimizu, Maria Heloisa Massola, Casarini, Dulce Elena, Seguro, Antonio Carlos, Patriarca, Giuliana, Coelho, Michella Soares, Dolnikoff, Miriam Sterman, Heimann, Joel Claudio
• Format: Article
• Language: English
• Subjects: Animals; Animals, Newborn; Behavioral psychophysiology; Biological and medical sciences; Blood Circulation - drug effects; Blood Pressure - drug effects; Body Weight - drug effects; Diseases of mother, fetus and pregnancy; Female; Fundamental and applied biological sciences. Psychology; Gynecology. Andrology. Obstetrics; Heart Rate - drug effects; Medical sciences; Peptidyl-Dipeptidase A - metabolism; Perinatal period; Placenta; Placenta - blood supply; Placenta - drug effects; Placenta - metabolism; Pregnancy; Pregnancy. Fetus. Placenta; Prenatal Exposure Delayed Effects; Psychiatry; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Rats; Rats, Wistar; Renin-angiotensin system; Renin-Angiotensin System - drug effects; Salt; Sodium Chloride, Dietary - pharmacology; Thiobarbituric Acid Reactive Substances - metabolism; Tumor Necrosis Factor-alpha - genetics; Tumor Necrosis Factor-alpha - metabolism; Uterus - drug effects; Uterus - metabolism
• ISSN: 0031-9384; 1873-507X
• DOI: 10.1016/j.physbeh.2008.05.011

Abstract A number of studies conducted in humans and in animals have observed that events occurring early in life are associated with the development of diseases in adulthood. Salt overload and restriction during pregnancy and lactation are responsible for functional (hemodynamic and hormonal) and structural alterations in adult offspring. Our group observed that lower birth weight and insulin resistance in adulthood is associated with salt restriction during pregnancy. On the other hand, perinatal salt overload is associated with higher blood pressure and higher renal angiotensin II content in adult offspring. Therefore, we hypothesised that renin–angiotensin system (RAS) function is altered by changes in sodium intake during pregnancy. Such changes may influence fetoplacental blood flow and thereby fetal nutrient supply, with effects on growth in utero and, consequently, on birth weight. Female Wistar rats were fed low-salt (LS), normal-salt (NS), or high-salt (HS) diet, starting before conception and continuing until day 19 of pregnancy. Blood pressure, heart rate, fetuses and dams' body weight, placentae weight and litter size were measured on day 19 of pregnancy. Cardiac output, uterine and placental blood flow were also determined on day 19. Expressions of renin–angiotensin system components and of the TNF-alpha gene were evaluated in the placentae. Plasma renin activity (PRA) and plasma and tissue angiotensin-converting enzyme (ACE) activity, as well as plasma and placental levels of angiotensins I, II, and 1–7 were measured. Body weight and kidney mass were greater in HS than in NS and LS dams. Food intake did not differ among the maternal groups. Placental weight was lower in LS dams than in NS and HS dams. Fetal weight was lower in the LS group than in the NS and HS groups. The PRA was greater in LS dams than in NS and HS dams, although ACE activity (serum, cardiac, renal, and placental) was unaffected by the level of sodium intake. Placental levels of angiotensins I and II were lower in the HS group than in the NS and LS groups. Placental angiotensin receptor type 1 (AT1 ) gene expression and levels of thiobarbituric acid reactive substances (TBARS) were higher in HS dams, as were uterine blood flow and cardiac output. The degree of salt intake did not influence plasma sodium, potassium or creatinine. Although fractional sodium excretion was higher in HS dams than in NS and LS dams, fractional potassium excretion was unchanged. In conclusion, fi